AJP - Lung Cellular and Molecular Physiology, Vol 269, Issue 6 884-L890, Copyright © 1995 by American Physiological Society
Mob-1 expression in IL-2-induced ARDS: regulation by TNF-alpha
L. F. Neville, F. Abdullah, P. M. McDonnell, P. R. Young, G. Z. Feuerstein and R. Rabinovici
Department of Surgery, Jefferson Medical College, Philadelphia 19107, USA.
We have recently established an animal model of adult respiratory distress
syndrome (ARDS)-like microvascular lung injury elicited by infusion of
human interleukin-2 (IL-2). Based on the pronounced, transcriptional
upregulation of multiple pro-inflammatory mediators in IL-2-induced ARDS,
differential display was applied to search for potentially novel genes in
this paradigm of lung injury. Differential display on total lung RNA
derived from IL-2-challenged rats presented a highly reproducible 3'-UTR
fragment profile in which a band (approximately 250 bp), termed B1, was
strongly induced. B1 cDNA sequence exhibited 99.14% homology to the 3'-UTR
of mob-1, a recently cloned gene belonging to the C-X-C chemokine
superfamily. Furthermore, Northern blot analysis showed that IL-2-induced
pulmonary mob-1 mRNA was expressed at time points before the onset of lung
injury and suppressed after TNF-alpha inhibition. These data imply that
lung mob-1 is a novel, highly inducible gene in a clinically relevant model
of ARDS and, based on its identification as a chemokine, could participate
in the development of lung injury.
